Figure 2

Pharmacological inhibition of CK2 causes apoptosis of AML cells. (A, B) Graphs showing the rate of apoptosis assessed by annexin V staining and FACS analysis in a panel of AML cell lines (NB4, ML2 and HL-60, for CX-4945 also Kasumi-1) treated with increasing concentrations of the CK2 inhibitors K27 (A) or CX-4945 (B). (C) Representative western blot analysis of PARP/cleaved PARP ratio expression in cell lysates from ML2 (top left panels), NB-4 (bottom panels) and HL-60 (top right panels) AML cell lines treated with increasing concentrations of K27. (D) Representative western blot analysis of PARP/cleaved PARP ratio and of phospho Ser13 CDC37 and total CDC37 expression in cell lysates from ML2 (top left panels), NB-4 (bottom left panels) and HL-60 (top right panels) and Kasumi-1 (bottom right panels) AML cell lines treated with increasing concentrations of CX-4945. βactin was used to ensure equal protein loading. (E) Graph summarizing the rate of apoptosis by annexin V staining and FACS analysis of blasts from AML patients (n = 7; p < 0.05) untreated (un) or treated with 5 μM CX-4945 for 18 hours. (F) Western blot analysis of apoptosis as indicated by PARP cleavage in AML blasts protein lysates taken from three AML patients. Proteins were made soon after collection, at time 0 and after 18 hours of culture untreated (Un) or upon exposure to CX-4945 5 μM. Data represent mean ± SD, n = 3. * indicates p < 0.05.